ArticleClinical and translational medicine2022
Mitochondrial GCN5L1 regulates glutaminase acetylation and hepatocellular carcinoma.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Amino Acid Metabolic Enzymes in Gastric Cancer: Roles and Mechanisms in Tumorigenesis and Progression.Oncology research · 2026Review
- The Immune Microenvironment in Liver Cancer: From Analysis to Targeting.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Acetylation of the Mitochondrial Chaperone GRP75 Governs ER-Mitochondrial Calcium Homeostasis and Hepatocyte Insulin Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Post-translational modifications in hepatocellular carcinoma: mechanisms and therapeutic potential.Medical oncology (Northwood, London, England) · 2025Review
- Targeting mitochondrial dysfunction to intervene in liver cancer.Cancer biology & medicine · 2025Review
- Inhibiting SSBP1 enhances ferroptosis and improves the effectiveness of sorafenib treatment for liver cancer.International journal of oncology · 2025Article
- GCN5L1 Aggravates Postherpetic Neuralgia Through Regulating Microglial Mitochondrial Fission-Fusion Homeostasis.Journal of cellular and molecular medicine · 2025Article
- The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis.Cellular and molecular life sciences : CMLS · 2025Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025Review
- Mitochondrial proteins: Potential pathophysiological mechanisms of malignant progression in HCC.PloS one · 2025Article
- Intricate effects of post-translational modifications in liver cancer: mechanisms to clinical applications.Journal of translational medicine · 2024Review
- Mitochondrial GCN5L1 acts as a novel regulator for iron homeostasis to promote sorafenib sensitivity in hepatocellular carcinoma.Journal of translational medicine · 2024Article
- Validation of GCN5L1/BLOC1S1/BLOS1 antibodies using knockout cells and tissue.The Biochemical journal · 2024Article
- A glimpse into novel acylations and their emerging role in regulating cancer metastasis.Cellular and molecular life sciences : CMLS · 2024Review
- Glutaminolysis is a Potential Therapeutic Target for Kidney Diseases.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Two Faces of Glutaminase GLS2 in Carcinogenesis.Cancers · 2023Review
- Discovery of Novel Mono-Carbonyl Curcumin Derivatives as Potential Anti-Hepatoma Agents.Molecules (Basel, Switzerland) · 2023Article
- BAIAP2L2 is a novel prognostic biomarker related to migration and invasion of HCC and associated with cuprotosis.Scientific reports · 2023Article
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundGlutaminolysis is a critical metabolic process that promotes cancer cell proliferation, including hepatocellular carcinoma (HCC). Delineating the molecular control of glutaminolysis could identify novel targets to ameliorate this oncogenic metabolic pathway. Here, we evaluated the role of general control of amino acid synthesis 5 like 1 (GCN5L1), a regulator of mitochondrial protein acetylation, in modulating the acetylation and activity of glutaminase to regulate HCC development.
methodsCell proliferation was determined by MTT, 2D and soft agar clone formation assays and orthotopic tumour assays in nude mice. GLS1/2 acetylation and activities were measured in cells and tumours to analyse the correlation with GCN5L1 expression and mTORC1 activation.
resultsHepatic GCN5L1 ablation in mice markedly increased diethylnitrosamine (DEN)-induced HCC, and conversely, the transduction of mitochondrial-restricted GCN5L1 protected wild-type mice against HCC progression in response to DEN and carbon tetrachloride (CCl
conclusionsOur study identified that glutaminase activity, rather than GLS1 or GLS2 expression, is the key factor in HCC development that activates mTORC1 and promotes HCC. In the Kaplan-Meier analysis of liver cancer, we found that HCC patients with high GCN5L1 expression survived longer than those with low GCN5L1 expression. Collectively, GCN5L1 functions as a tumour regulator by modulating glutaminase acetylation and activity in the development of HCC.
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